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KMID : 0923620130130040123
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Immune Network
2013 Volume.13 No. 4 p.123 ~ p.132
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Metformin Down-regulates TNF-α Secretion via Suppression of Scavenger Receptors in Macrophages
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Hyun Bo-Bae
Shin Seul-Mee
Lee Ae-Ri
Lee Sung-Won
Song Young-Cheon
Ha Nam-Joo
Cho Kyung-Hea
Kim Kyung-Jae
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Abstract
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Obesity is consistently increasing in prevalence and can trigger insulin resistance and type 2 diabetes. Many lines of evidence have shown that macrophages play a major role in inflammation associated with obesity. This study was conducted to determine metformin, a widely prescribed drug for type 2 diabetes, would regulate inflammation through down- regulation of scavenger receptors in macrophages from obesity-induced type 2 diabetes. RAW 264.7 cells and peritoneal macrophages were stimulated with LPS to induce inflammation, and C57BL/6N mice were fed a high-fat diet to generate obesity-induced type 2 diabetes mice. Metformin reduced the production of NO, PGE2 and pro-inflammatory cytokines (IL-1β, IL-6 and TNF-α) through down-regulation of NF-κB translocation in macrophages in a dose-dependent manner. On the other hand, the protein expressions of anti-inflammatory cytokines, IL-4 and IL-10, were enhanced or maintained by metformin. Also, metformin suppressed secretion of TNF-αand reduced the protein and mRNA expression of TNF-α in obese mice as well as in macrophages. The expression of scavenger receptors, CD36 and SR-A, were attenuated by metformin in macrophages and obese mice. These results suggest that metformin may attenuate inflammatory responses by suppressing the production of TNF-α and the expressions of scavenger receptors.
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KEYWORD
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Metformin, Obesity-induced inflammation, TNF-α, Scavenger receptors
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